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[2] [6] [13] [14] As the drug begins to take effect, the brain becomes flooded with serotonin which can then become depleted within 3–6 hours following consumption. [14] It has also been shown that an enzyme required to synthesize serotonin becomes deactivated, therefore, inhibiting the brain's replenishment of used serotonin. [ 14 ]
Sertraline, sold under the brand name Zoloft among others, is an antidepressant medication of the selective serotonin reuptake inhibitor (SSRI) class [10] used to treat major depressive disorder, generalized anxiety disorder, social anxiety disorder, obsessive–compulsive disorder (OCD), panic disorder, and premenstrual dysphoric disorder. [11]
Despite their side effects, some tricyclic antidepressants may be effective for improving depression symptoms when other, newer medications aren’t effective. Atypical antidepressants.
[181] [182] Discontinuation effects appear to be less for fluoxetine, perhaps owing to its long half-life and the natural tapering effect associated with its slow clearance from the body. One strategy for minimizing SSRI discontinuation symptoms is to switch the patient to fluoxetine and then taper and discontinue the fluoxetine.
For instance, you might start off taking Zoloft but eventually switch to Prozac because its side effects feel less severe. Whatever the reason, switching from one medication to another is totally ...
Research shows that between 25 and 73 percent of people who used antidepressants like Zoloft to treat depression, anxiety and other conditions experience intimate side effects. Basically ...
Zoloft – an antidepressant of the SSRI class; Zonegran (zonisamide) – an anticonvulsant used to treat other seizures; Zulresso (brexanolone) – a GABA modulator antidepressant; Zyban (bupropion) – same active ingredient as Wellbutrin, but marketed as a smoking cessation aid
In humans the effects of excess serotonin were first noted in 1960 in patients receiving an MAOI and tryptophan. [54] The syndrome is caused by increased serotonin in the CNS. [6] It was originally suspected that agonism of 5-HT 1A receptors in central grey nuclei and the medulla oblongata was responsible for the development of the syndrome. [55]